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Midbrain Infarction Presenting with Webers

Syndrome and Central Facial Palsy: A Case Report
ARTICLE in NOROPSIKIYATRI ARSIVI JANUARY 2009
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Case Report / Olgu Sunumu

197

Midbrain Infarction Presenting with Webers Syndrome and

Central Facial Palsy: A Case Report
Orta Beyin nfarktna Bal Gelien Weber Sendromu ve Santral Fasyal Parezi: Olgu Sunumu
Demet LHAN ALGIN, Figen TAER*, Sayime AYDIN**, Elif AKSAKALLI***
Dumlupnar University Faculty of Medicine, Department of Neurology, Ktahya
*Dumlupnar University Faculty of Medicine, Department of Anatomy, Ktahya
**Dumlupnar University Faculty of Medicine, Department of Ophthalmology, Ktahya
***Dumlupnar University Faculty of Medicine, Department of Physical therapy and Rehabilitation, Ktahya, Turkey

ABSTRACT
Weber's syndrome is a distinctive brainstem disease characterized by ipsilateral
3rd nerve palsy with contralateral hemiplegia and is due to an intrinsic or
extrinsic lesion in the ventral midbrain. To date, there is limited literature
concerning Weber's syndrome associated with central facial palsy, but none
was demonstrated with comprehensive explanation. We report a rare case
presented with Webers syndrome and central facial palsy caused by infarction
of ventromedial crural region of the mesencephalon.
The patient was a 68-year-old woman who developed central type facial palsy on
right side, and complete left 3rd nerve palsy, right hemiparesis and paresthesia
with deep sensory disturbance of right upper and lower extremities.
A T2 weighted cranial MRI showed an acute infarct in the left ventromedial
crural region of the mesencephalon and this lesion was presumed to involve both
the corticospinal and corticobulbar tracts. This report demonstrates an
extremely rare case of crossed hemiplegia with oculomotor and facial nerve
palsy due to an infarct in the upper part of the midbrain as documented by the
MRI scan. The other interesting feature to note in our report is that the patient
completely recovered six months later. This indicates that some of these patients
may have a good prognosis. (Archives of Neuropsychiatry 2009; 46: 197-9)
Key words: Webers syndrome; facial nerve; oculomotor nerve; corticobulbar
tract; midbrain infarct

Case
A 68-year-old woman was admitted to the Dumlupinar
University Hospital because of central type facial palsy on right
side, right hemiparesis, and paresthesia with deep sensory
disturbance of right upper and lower extremities (Figure 1A). She
had ptosis, midriasis and lateral-inferior deviation of the left eye
due to oculomotor nerve palsy (Figure 1B).

ZET
Weber sendromu ipsilateral 3. sinir parezisi ve kontrlateral hemipleji ile karakterize zellikli bir beyinsap hastaldr ve ventral orta beyindeki intrinsik veya
ekstrinsik lezyona bal olarak geliir. Bugne kadar, santral fasyal parezi ile
ilikili Weber sendromu konusunda snrl sayda literatr mevcuttur, ancak hibiri kapsaml bir aklama ile sunulmamtr. Mesensefalonun ventromedial
krural blgesinin infarktna bal gelien Weber sendromu ve santral fasyal parezi ile bavuran nadir bir olgudan bahsedilmektedir.
Olgu, sa santral fasyal parezi, sol 3. kranial sinir parezisi, sa hemiparezi, sa
st ve alt ekstremitede derin duyu bozukluu ile birlikte parestezi gelien 68 yanda bir kadn hasta idi.
T2 arlkl kranial MRGde mezensefalonun sol ventromedial krural blgesinde
akut infarkt grld ve bu lezyonun kortikospinal ve kortikobulbar traktuslar birlikte etkiledii dnld. Bu sunumda orta beyinin st ksmndaki infarkta bal
okulomotor ve fasyal parezi ile beraber apraz hemipleji gelien nadir bir olgu
MRG bulgularyla beraber tartlmtr. Hastann alt ay sonra tamamen iyilemi
olmas da ayrca belirtilmesi gereken ilgin bir zelliktir ki bu da hastalarn bir
ksmnn iyi bir prognoza sahip olabileceini gstermektedir. (Nropsikiyatri
Arivi 2009; 46: 197-9)
Anahtar kelimeler: Weber sendromu, fasyal sinir, okulomotor sinir, kortikobulber traktus, mezensefalon infarkt

Our patient noticed weakness of the right arm and leg and
diplopia on waking in the morning. She had been diabetic and
hypertensive for the past 20 years. Her medications included
gliclazide, metformin and insulin. On admission she was alert
and had a blood pressure of 155/75 mm/Hg with no arrhythmia.
Neurological examination revealed a conscious individual with
normal higher cortical functions.

Address for Correspondence/Yazma Adresi: Dr. Demet lhan Algn, Dumlupnar University Faculty of Medicine, Department of Neurology, Ktahya, Turkey
E-mail: ilhandemet@gmail.com Received/Geli tarihi: 20.05.2009 Accepted/Kabul tarihi: 22.09.2009
Archives of Neuropsychiatry, Published by Galenos Publishing. All rights reserved. / Nropsikiyatri Arivi Dergisi, Galenos Yaynclk tarafndan baslmtr. Her hakk sakldr.

198

Algn et al.
Midbrain Infarction Presenting with Webers Syndrome and Central Facial Palsy: A Case Report

Cranial examination revealed complete left 3rd nerve palsy and

normal ocular fundi. The strength of the frontalis and orbicularis
oculi muscles was well preserved, but she had a right lower facial
weakness with mild flattening of the right nasolabial fold and
paralytic dysarthria. Motor system showed right-sided spastic
weakness with grade 4/5 power. Deep tendon reflexes were brisk
on the right side with upgoing plantar response. Initial computerized
tomography (CT) scan was normal. Cranial magnetic resonance
imaging (MRI) performed 10 days after the onset showed an
infarction in the left ventromedial part of the upper mesencephalon
and old multiple chronic lacunar infarctions in the deep white
matter of the cerebral hemispheres (Figure 1C).
Over the next week her hemiparesis resolved completely and
her diplopia was getting better. Two weeks later, she was
discharged with normal neurological findings.

Figure 1A. Central type facial palsy on right side

Figure 1B. Extraocular movements in 9 cardinal positions

Archives of Neuropsychiatry 2009; 46: 197-9

Nropsikiyatri Arivi 2009; 46: 197-9

Discussion
Weber's syndrome was described by the German physician
Hermann Weber in 1863 (1). The clinical findings of classic
Weber's syndrome include an ipsilateral oculomotor nerve palsy
and a contralateral limb weakness due to a lesion in the
midbrain (crus cerebri).
Most of the muscles of the eye innervates by the oculomotor
nerve. The motor nucleus of this nerve is located at the upper
mesencephalic level of brainstem. Nerve nascicles run forward
and laterally through the red nuclei and get closer at the
inter-peduncular fossa. So nuclei and fascicles of the oculomotor
nerve are expanding a relatively wide area within midbrain.
Therefore midbrain lesions generally lead to partial third nerve
palsy. It enters the orbit through the superior orbital fissure after
come out from the midbrain and branching into upper and lower
fibers. While the levator palpebrae superioris and superior
rectus muscles were innervated by the upper branch, the
medial rectus, the inferior rectus, and the inferior oblique
muscles were innervated by the lower branch (2-4).

Figure 1C. T2-weighted cranial magnetic resonance imaging shows an

infarction at the left ventromedial part of the upper mesencephalon

Archives of Neuropsychiatry 2009; 46: 197-9

Nropsikiyatri Arivi 2009; 46: 197-9

Algn et al.
Midbrain Infarction Presenting with Webers Syndrome and Central Facial Palsy: A Case Report

The preganglionic parasympathetic fibers of the 3rd nerve

which are transported by the nerve to the inferior oblique
muscle arrive to the ciliary ganglion and from here the
post-ganglionic parasympathetic fibers emerge. The ciliary
muscle and the muscles of the iris are innervated by these
post-ganglionic parasympathetic fibers. The nerve fibers to
levator palpebrae muscle and the pupilloconstrictor fibers for
the muscles of the iris are located in a superficial and dorsal
position on the nerve relaying in the ciliary ganglion. Before
external ophthalmoplegia develops, a fixed dilated pupil is often
the first sign of 3rd nerve (oculomotor) compression, and ptosis
the second, upon this anatomical characteristic (5).
The clinical manifestation of the patients with isolated
mesencephalic infarct was shown up nuclear or fascicular
oculomotor nerve palsy and contralateral motor deficits (6,7).
In patients with isolated mesencephalic infarct, the clinical
picture was dominated by nuclear or fascicular third-nerve palsy
and contralateral motor deficits (6,8).
On the other hand the corticobulbar tract (CBT) is commonly
used to describe the pathway taken by motor fibers innervating
the cranial nerve nuclei, especially trigeminal, facial, hypoglossal motor nuclei, nucleus ambiguus, and spinal accessory
nucleus. The oculomotor, trochlear and abducens
nuclei receive no input from the CBT. The cell bodies of primary
motor neurons are located in primary motor cortex (9).
The motor nucleus of the facial nerve, which supplies the
muscles of the facial expression, is located at the lower pontine
level, dorsolaterally in the caudal pons (4). The CBT fibers that
connect the motor cortex with the facial nucleus provide
strongly unilateral innervation to the contralateral lower facial
muscles and bilateral innervation to the upper facial muscles.
The facial CBT fibers descend at the ventromedial region of the
crus cerebri, near the corticospinal tract (10).
The clinical manifestations of midbrain infarcts mostly show
the location of the lesion directly, but these features could not
always match with classical syndromes which described
previously in the literature, just like our case that we present in
this report (11).
Posterior cerebral artery branch disease may be caused by
occlusion of the arterial branch with atherothrombotic plaque
(4). In these cases, hypertension is a major risk factor, as seen in
our patient (10).
Kumral et al. presented the topographic and clinical
distribution of the acute posterior circulation infarcts involving
mesencephalon. They described four patients with Webers
syndrome and central facial palsy due to isolated midbrain
infarct around ventromedial crural region within 41 patients with
mesencephalic infarction. These were the only cases in the
literature identical to our patient (6).
Some minor infarctions at the midbrain which resulted in
localized paralysis like weakness of a single extraocular muscle
(12), isolated contralateral superior rectus palsy (13) have been
demonstrated previously. Some interesting cases, such as
presence of left oculomotor nerve palsy with normal pupil and
right hemiparesis, were described. An ischemic lesion of the
lower midbrain, which corresponds to the motor nucleus of the

199

oculomotor nerve, was demonstrated in this case (3).

Terao et al. reported two patients with contralateral central
facial paralysis and hemiparesis of the limbs, resulted from
unilateral ventromedial medullary infarction (14). According to
these cases, they described the course of the facial corticobulbar
tract as consisting of looping fibers that descend at least to the
medullary level and then decussate. In another study with larger
group (70 patients), they attempted to further clarify the course
and the distribution of the facial corticobulbar tract (10). But the
authors could not coincide with third nerve palsy or Webers
syndrome within these central facial palsy patients.
Finally, this report demonstrates an extremely rare case of
crossed hemiplegia with oculomotor and facial nerve palsy due
to an infarct in the upper part of the midbrain as documented by
the MRI scan. The other interesting feature to note in our report
is that the patient completely recovered six month later. This
indicates that some of these patients may have a good prognosis.

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